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1.
Nat Prod Res ; 34(7): 975-980, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30600724

RESUMO

An ongoing chemical investigation on n-BuOH extract of roots and rhizomes of Helleborus thibetanus afforded three new spirostanol glycosides (1-3). Their structures were elucidated by extensive analysis of 1 D, 2 D NMR spectra, together with IR and MS methods and acid hydrolysis. This is the first report of the isolation of spirostanol glycoside with xylose at C-24 of the aglycone in Helleborus.


Assuntos
Glicosídeos/isolamento & purificação , Helleborus/química , Espirostanos/química , Glicosídeos/química , Hidrólise , Espectroscopia de Ressonância Magnética , Estrutura Molecular , Raízes de Plantas/química , Rizoma/química , Saponinas/química
2.
Front Biosci (Landmark Ed) ; 21(5): 1039-51, 2016 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-27100489

RESUMO

Endothelial cell dysfunction is the primary cause of microvascular complications in diabetes. Diazoxide enables beta cells to rest by reversibly suppressing glucose-induced insulin secretion by opening ATP-sensitive K+ channels in the beta cells. This study investigated the role of diazoxide in wound healing in mice with streptozotocin (STZ)-induced diabetes and explored the possible mechanisms of its effect. Compared to the controls, mice with STZ-induced diabetes exhibited significantly impaired wound healing. Diazoxide treatment (30 mg/kg/d, intragastrically) for 28 days accelerated wound closure and stimulated angiogenesis in the diabetic mice. Circulating endothelial progenitor cells (EPCs) increased significantly in the diazoxide-treated diabetic mice. The adhesion, migration, and tube formation abilities of bone marrow (BM)-EPCs were impaired by diabetes, and these impairments were improved by diazoxide treatment. The expression of both p53 and TSP-1 increased in diabetic mice compared to that in the controls, and these increases were inhibited significantly by diazoxide treatment. In vitro, diazoxide treatment improved the impaired BM-EPC function and diminished the increased expression of p53 and TSP-1 in cultured BM-EPCs caused by high glucose levels. We conclude that diazoxide improved BM-EPC function in mice with STZ-induced diabetes, possibly via a p53- and TSP-1-dependent pathway.


Assuntos
Diazóxido/farmacologia , Células Endoteliais/efeitos dos fármacos , Cicatrização/efeitos dos fármacos , Animais , Apoptose/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Experimental/patologia , Diabetes Mellitus Experimental/fisiopatologia , Células Endoteliais/patologia , Células Endoteliais/fisiologia , Glucose/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Neovascularização Fisiológica/efeitos dos fármacos , Canais de Potássio/agonistas , Células-Tronco/efeitos dos fármacos , Células-Tronco/patologia , Células-Tronco/fisiologia , Trombospondina 1/metabolismo , Proteína Supressora de Tumor p53/metabolismo , Cicatrização/fisiologia
4.
Radiat Res ; 181(6): 666-71, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24828112

RESUMO

Radiation-induced gastrointestinal syndrome occurs when the body is exposed to a high dose of radiation. Currently, safe and effective radioprotectants are not available. Apoptosis was reported to play a primary role in radiation-induced injury. Recent evidence suggests that stimulation of α7 nicotinic acetylcholine receptor (α7nAChR) prevents cell death by inhibition of apoptosis. In this study, we demonstrated that a single dose of PNU282987 (100 µg/kg, i.p.), a selective α7nAChR agonist, protected mice from intestinal injury and significantly improved survival when administered prior to lethal 8 Gy total body irradiation. In vitro, PNU282987 protected against 8 Gy radiation-induced cell death in human umbilical venous endothelial cells by inhibiting apoptosis. We conclude that activation of α7nAChR may provide a new therapeutic pathway for the treatment of radiation-induced damage and mortality.


Assuntos
Intestinos/efeitos da radiação , Lesões por Radiação/tratamento farmacológico , Lesões por Radiação/metabolismo , Ferimentos e Lesões/metabolismo , Receptor Nicotínico de Acetilcolina alfa7/genética , Animais , Apoptose/efeitos da radiação , Regulação da Expressão Gênica/efeitos da radiação , Humanos , Intestinos/efeitos dos fármacos , Masculino , Camundongos , Lesões por Radiação/genética , Irradiação Corporal Total , Ferimentos e Lesões/patologia , Receptor Nicotínico de Acetilcolina alfa7/biossíntese
5.
Neurobiol Learn Mem ; 114: 10-5, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-24752150

RESUMO

Previous evidence suggests that a high-salt (HS) diet may increase oxidative stress and contribute to the development of hypertension that is already present. Oxidative stress is thought to play a critical role in the development of neurodegenerative diseases. Lower dietary sodium intake putatively contributes to a lower rate of cognitive impairment; however, the specific effects of HS diet on cognitive function remain poorly understood. In this work, C57BL/6J mice were administered a normal-salt (NS) diet (0.4% NaCl) or a HS diet (7.0% NaCl) for 12 weeks, and cognitive ability and oxidative stress in the brain were measured. It was found that the HS diet significantly impaired retention of spatial memory. Additionally, superoxide anion production in the hippocampus was significantly increased in the HS diet mice compared with that in the NS mice. Interestingly, the antioxidant defense capacities for HS diet mice were markedly reduced in the hippocampus, but not in the cerebral cortex, compared with the NS mice. Taken together, these data demonstrate that HS diet directly impairs retention of spatial memory, which may be related to the increased oxidative stress observed in the hippocampus.


Assuntos
Cognição/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Cloreto de Sódio na Dieta/administração & dosagem , Memória Espacial/efeitos dos fármacos , Animais , Cognição/fisiologia , Transtornos Cognitivos/metabolismo , Hipocampo/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Memória Espacial/fisiologia , Superóxidos/metabolismo
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